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. Author manuscript; available in PMC: 2019 Jun 19.
Published in final edited form as: J Mammary Gland Biol Neoplasia. 2018 Aug 9;23(4):249–267. doi: 10.1007/s10911-018-9407-1

Fig 5. CXCR2 knockdown in 144epi cells inhibits Tgfbr2FspKO fibroblasts mediated progression of 144epi mammary lesions.

Fig 5.

A. Flow cytometry analysis of CXCR2 in Parental (Par) or 144epi cells stably expressing control shRNA (Ctrl) or CXCR2 shRNAs (F-6, G-1). Percentage of positive cells are shown. B. CXCL1 ELISA of cultured 144epi cells. C-F. Tgfbr2FspKO fibroblasts were co-transplanted with control or CXCR2 deficient 144epi cells. Mammary tissues were analyzed by H&E stain (C), tumor mass (D), Ki67 (E), or Gr-1 expression (F). Statistical analysis was determined by One Way ANOVA followed by Bonferroni post-hoc comparison of F-6 and G-1 with control shRNA. Statistical significance was determined by p <0.05. *p<0.05; **p<0.01, ***p<0.001, ns=not significant. Scale bar=200 microns. n=12 for parental 144epi: Tgfbr2FspKO, n=7 for 144epi: Control shRNA, n=6 for 144epi:F-6, n=6 for 144epi:G-1. Flow cytometry experiments were performed 3 times. Mean±SEM are shown.